ahad mokhtarzadeh

MicroRNAs are considered the main regulators of many biological processes, such as cell proliferation and apoptosis, through controlling the expression of various genes. Therefore, changes in the expression of microRNAs play an important role in the occurrence of various diseases, including cancer. Glioblastoma multiforme is the most aggressive tumor of the central nervous system, whose prognosis is still poor despite progress in various treatment methods. In addition, glioblastoma is a multifactorial disease characterized by heterogeneity, which is the main reason for its resistance to common treatments. Identification of microRNAs and determination of the decrease or increase in their expression in glioblastoma can be considered a fast and minimally invasive diagnostic method and a promising treatment approach. Expression of miR-143/145 gene cluster is decreased in glioblastoma. Studies on glioblastoma have indicated that a decreased expression of the miR-143/145 cluster is associated with poor prognosis in patients. Research has suggested that upregulation of both microRNAs leads to reduced proliferation and invasion of glioblastoma cells.

In this study, searches were conducted in the scientific resource databases Google Scholar, PubMed, and Scopus using the keywords MicroRNA, Glioblastoma, miR-143, and miR-145 without any time restrictions and employing the logical operators NOT, OR, and AND.

Based on the research articles, a summary of the role of miR-143/145 in glioblastoma was provided.

This review showed that microRNAs participate in many cell signaling pathways involved in tumorigenesis and progression of glioblastoma, including proliferation, differentiation, programmed cell death, metastasis, angiogenesis, and drug resistance. Therefore, microRNAs can be used as diagnostic and therapeutic biomarkers in glioblastoma.

 MicroRNAs (miRNAs) are a group of small regulatory non-coding RNAs, which are dysregulated through tumor progression. let-7 and MIR-145 are both tumor suppressor microRNAs that are downregulated in a wide array of cancers including colorectal cancer (CRC).

 This study was aimed to investigate the effect of simultaneous replacement of these two tumor suppressor miRNAs on proliferation, apoptosis, and migration of CRC cells. HCT-116 with lower expression levels of hsa-let-7a-3p and MIR-145-5p was selected for functional investigations. The cells were cultured and transfected with hsa-let-7a and MIR-145, separately and in combination. Cell viability and apoptosis rates were assessed by MTT assay and flow cytometry, respectively. Cell cycle status was further evaluated using flow cytometry and qRT-PCR was employed to evaluate gene expression.

 The obtained results showed that exogenous overexpression of MIR-145 and hsa-let-7a in HCT-116 cells could cooperatively decrease CRC cell proliferation and induce sub-G1 cell cycle arrest. Moreover, hsa-let-7a and MIR-145 co-transfection significantly increased apoptosis induction compared to separate transfected cells and control through modulating the expression levels of apoptosis-related genes including Bax, Bcl-2, P53, Caspase-3, Caspase-8, and Caspase-9. Furthermore, qRT-PCR results illustrated that hsa-let-7a and MIR-145 combination more effectively downregulated MMP-9 and MMP-2 expression, as the important modulators of metastasis, compared to the controls.

 Taken together, considering that exogenous overexpression of MIR-145 and hsa-let-7a showed cooperative anti-cancer effects on CRC cells, their combination may be considered as a novel therapeutic strategy for the treatment of CRC.

 As the most common aggressive primary brain tumor, glioblastoma is inevitably a recurrent malignancy whose patients’ prognosis is poor. miR-143 and miR-145, as tumor suppressor miRNAs, are downregulated through tumorigenesis of multiple human cancers, including glioblastoma. These two miRNAs regulate numerous cellular processes, such as proliferation and migration. This research was intended to explore the simultaneous replacement effect of miR-143, and miR-145 on in vitro tumorgenicity of U87 glioblastoma cells.

 U87 cells were cultured, and transfected with miR-143-5p and miR-145-5p. Afterward, the changes in cell viability, and apoptosis induction were determined by MTT assay and Annexin V/PI staining. The accumulation of cells at the cell cycle phases was assessed using the flow cytometry. Wound healing and colony formation assays were performed to study cell migration. qRT-PCR and western blot techniques were utilized to quantify gene expression levels.

 Our results showed that miR-143-5p and 145-5p exogenous upregulation cooperatively diminished cell viability, and enhanced U-87 cell apoptosis by modulating Caspase-3/8/9, Bax, and Bcl-2 protein expression. The combination therapy increased accumulation of cells at the sub-G1 phase by modulating CDK1, Cyclin D1, and P53 protein expression. miR-143/145-5p significantly decreased cell migration, and reduced colony formation ability by the downregulation of c-Myc and CD44 gene expression. Furthermore, the results showed the combination therapy of these miRNAs could remarkably downregulate phosphorylated-AKT expression levels.

 In conclusion, miR-143 and miR-145 were indicated to show cooperative anti- cancer effects on glioblastoma cells via modulating AKT signaling as a new therapeutic approach.

Prostate cancer (PC) is one of the most commonly diagnosed malignancies among men worldwide. Paclitaxel is a chemotherapeutic agent widely used to treat different types of cancer. Recent studies revealed miRNAs control various genes that influence the regulation of many biological and pathological processes such as the formation and development of cancer, chemotherapy resistance, etc. Between three PC cell lines (PC3, DU-145, LNCAP), PC3 showed the lowest miR-145 expression and was chosen for experiments. PC3 cells were treated with paclitaxel and miR-145 separately or in combination. To measure the cell viability, migratory capacity, autophagy, cell cycle progression, and apoptosis induction, the MTT assay, wound-healing assay, and Annexin V/PI apoptosis assay were used, respectively. Moreover, quantitative real-time PCR (qRT-PCR) was employed to measure the expression level of genes involved in apoptosis, migration, and stemness properties. Obtained results illustrated that miR-145 transfection could enhance the sensitivity of PC3 cells to paclitaxel and increase paclitaxel-induced apoptosis by modulating the expression of related genes, including Caspase-3, Caspase-9, Bax, and Bcl-2. Also, results showed combination therapy increased cell cycle arrest at the sub-G1 phase. miR-145 and paclitaxel cooperatively reduced migration ability and related-metastatic and stemness gene expression, including MMP-2, MMP-9, CD44, and SOX-2. In addition, combination therapy can suppress MDR1 expression. These results confirmed that miR-145 combined with paclitaxel cooperatively could inhibit cell proliferation and migration and increase the chemosensitivity of PC3 cells compared to mono treatment. So, miR-145 combination therapy may be used as a promising approach for PC treatment.

Gastric cancer (GC) is the third leading cause of cancer-related death worldwide. microRNAs are a group of regulatory non-coding RNAs that are involved in GC progression. miR-145 as a tumor suppressor and miR-21 as an oncomiR were shown to be dysregulated in many cancers including GC. This research aimed to enhance the expression of miR-145 while reducing the expression of miR- 21 and examine their impact on the proliferation, apoptosis, and migration of GC cells.

KATO III cells with high expression levels of miR-21-5p and low expression of miR-145-5p were selected. These cells were then transfected with either miR-145-5p mimics or anti-miR-21-5p, alone or in combination. Afterward, the cell survival rate was determined using the MTT assay, while apoptosis induction was investigated through V-FITC/PI and DAPI staining. Additionally, cell migration was examined using the wound healing assay, and cell cycle progression was analyzed through flow cytometry. Furthermore, gene expression levels were quantified utilizing the qRT-PCR technique.

The study's findings indicated that the co-replacement of miR-145-5p and anti-miR-21- 5p led to a decrease in cell viability and the induction of apoptosis in GC cells. This was achieved via modulating the expression of Bax and Bcl-2, major cell survival regulators. Additionally, the combination therapy significantly increased sub-G1 cell cycle arrest and reduced cell migration by downregulating MMP-9 expression as an epithelial-mesenchymal transition marker. This study provides evidence for the therapeutic possibility of the combination of miR-145-5p and anti-miR- 21-5p and also suggests that they could inhibit cell proliferation by modulating the PTEN/AKT1 signaling pathway.

Our research revealed that utilizing miR-145-5p and anti-miR-21-5p together could be a promising therapeutic approach for treating GC.

Production of functional recombinant antibody fragments in the periplasm of E. coli isa prerequisite step to achieve sufficient reagent for preclinical studies. Thus, the cost-effectiveand lab-scale production of antibody fragments demands the optimization of culture conditions.

The culture conditions such as temperature, optical density (OD600) at induction,induction time, and IPTG concentration were investigated to optimize the functional expressionof a phage-derived scFv molecule using a design of experiment (DoE). Additionally, the effectsof different culture media and osmolyte supplements on the expression yield of scFv wereexamined.

The developed 2FI regression model indicated the significant linear effect of theincubation temperature, the induction time, and the induction OD600 on the expression yieldof functional scFv. Besides, the statistical analysis indicated that two significant interactions ofthe temperature/induction time and the temperature/induction OD600 significantly interplay toincrease the yield. Further optimization showed that the expression level of functional scFvwas the most optimal when the cultivation was undertaken either in the TB medium or in thepresence of media supplements of 0.5 M sorbitol or 100 mM glycine betaine.

In the present study, for the first time, we successfully implemented DoE tocomprehensively optimize the culture conditions for the expression of scFv molecules in aphage antibody display setting, where scFv molecules can be isolated from a tailor-made phageantibody library known as “Human Single Fold scFv Library I.”

microRNA‐193a‐5p is one of the well-known tumor suppressor miRNAs in the body but in many cases, its expression became reduced in patients suffering from gastric cancer (GC). The main purpose of this study was to restore the function of this miRNA in human GC cells and investigating the effects of enhanced expression of miR‐193a‐5p on proliferation, apoptosis, and migration of GC cells upon in vitro transfection.

The KATO III gastric cancer cells were treated with 100 nM of miR‐193a‐5p or negative control sequences. Following that, the MTT assay, flow cytometry assay, and wound-healing assay were applied to estimate the impacts of enhanced expression of this miRNA on the viability, apoptosis, and migration rate of the cells, respectively. Moreover, the total RNA was isolated and alterations in the mRNA expression ratio of migratory genes were measured by qRT-PCR techniques.

The findings designated that enhanced expression of miR‐193a‐5p suppressed the migratory ability of the cells, but had no significant effects on cell survival or apoptosis of the transfected cells. In addition, this inhibitory function of miR‐193a‐5p on the migration rate of the KATO III cell line occurs with concurrent suppression of vimentin and MMP-9 gene expression.

It can be concluded that miR‐193a‐5p negatively influences the migratory ability of the cancerous cells and restoring its effects can be regarded as a promising target of future therapeutic interventions, especially for GC metastasis.

Glioblastoma multiforme (GBM) is the most invasive type of cancer which starts inside the brain. GBM cells were found to have similar properties to glioblastoma cancer stem cells. CD44 can be used as a marker of the cancer stem cells in a subset of glioblastoma tumor cells. Recent studies showed that CD44 is involved in developing cancer cells via the protein kinase B (PKB or AKT) signaling pathway. Therefore, this study aimed to investigate the CD44 mRNA silencing effects on the glioblastoma cell cycle via AKT signaling pathway.

To determine CD44 expression in the samples of the patients with GBM, we used the analysis of data extracted from TCGA database. qRT-PCR and western blotting were used to evaluate the expression level of genes and proteins. Different cell cycles were evaluated by DAPI staining and flow cytometry.

Bioinformatics results showed that CD44 expression level in GBM tumor samples is higher than in normal samples. Effects of poly (ethylene imine)-polyethylene glycol (PEI-PEG)-loaded CD44 siRNA in cell cycle showed that CD44 silencing could inhibit cell cycle in G0-G1 phase by more than 20% compared to the negative control (P < 0.05). Furthermore, PEI-PEG-loaded CD44 siRNA reduces the expression of cyclin D1 and CKD-4. According to our findings, this structure also prevented AKT phosphorylation at Thr-308 and Ser-473.

Our results suggest that PEI-PEG-loaded CD44 siRNA may attenuate the cell cycle by suppressing AKT signaling pathway.

A series of cases of pneumonia occurred in China in late 2019. For this type of coronavirus, the World Health Organization (WHO) formally identified the condition as a coronavirus disease 2019 (COVID-19). They announced that this disease is the recent main concern of health problems in the world. Transfer of this novel coronavirus (nCoV) from human to human exists predominantly among family members, who have close contact with each other. This review article is provided based on the recent findings of COVID-19, which were retrieved by searching PubMed, Google Scholar, Scopus, and Web of Science until December 2020. Here, we highlighted the coronaviruses types, COVID-19 symptoms, epidemiology of the disease, transmission ways, and nCoV related pneumonia pathogenesis and continue with characteristic features and treatment methods. While no approved treatments are available for this type of infection therapy but several drugs may have potential benefits. It seems that identifying the detailed characteristics of the novel coronavirus disease offers the foundation for further research into the production of effective anti-COVID-19 drugs and vaccines.

The expression of miR-146a-5p and miR-193a-5p in colorectal cancer (CRC) is associated with cancer development, metastasis, and reduced survival rate of the tumor-suffered subjects. This examination aimed to assess the impact of these microRNAs (miRNAs) in CRC and their mechanisms in the proliferation and migration of cancer cells.

miR-146a-5p and -193a-5p were transfected into the HT-29 cell line and assessed their impact on metastasis-related genes. The synergistic effects of these miRNAs on migration were evaluated by wound healing approach. To assess the influence of these miRNAs on the proliferation of and apoptosis of cells, the MTT test, annexin V staining test, and DAPI staining test were done. Then, the protein expression of extracellular-signal-regulated kinase (ERK) and phosphorylated ERK (p-ERK) were investigated.

miR-146a-5p and-193a-5p could inhibit the CRC cells proliferation, and could synergistically induce apoptosis in CRC cells, and also repressed cell migration, and could reduce p-ERK expression.

miR-146a-5p and-193a-5p have an important role in cell viability and proliferation via ERK signaling pathway. Thus, the simultaneous use of these miRNAs may be suggested as a probable therapeutic strategy in this cancer therapy.

In this study, the inhibitory effects of polyethylene imine glycol (PEI-PEG)/ CD44 siRNA nanostructures on the proliferation, invasion, and apoptosis of U87MG GBM cancer cell line, as well as the expression levels of ALDH1, RANKL, and NOTCH1 were evaluated.

In this experimental study, PEI-PEG/ CD44 siRNA nanoparticles were synthesized and characterized by atomic force microscopy (AFM), evaluation of size and zeta potential, and Fourier transform infrared (FTIR) spectroscopy. The MTT assay was adopted to evaluate the cytotoxicity of the nanoparticles. The expression levels of target genes were assessed by qRT-PCR. Flow cytometry was used for apoptosis evaluation and Trans well matrigel assay and scratch-migration were employed for investigating the invasion and migration of glioma cells.

The size and zeta potential of PEI-PEG were influenced after CD44 siRNA loading. PEI-PEG loaded with CD44 siRNAs resulted in significant inhibition of glioblastoma cell line in the concentration of 60 pmol (P<0.05). In addition, transfection of glioma cells with CD44 siRNA led to significant downregulation of ALDH1, NOTCH1, and RANKL1 (P<0.05). Transfection of this siRNA also resulted in significant suppression of invasion and migration (P<0.05).

PEI-PEG could effectively form the polyplex in combination with siRNA, be transfected into the U87MG glioma cancer cell line, and inhibit the proliferation, invasion and migration of glioma cells via suppression of ALDH1 and NOTCH1, as well as RANKL1 expression levels

Colorectal cancer (CRC) remains a universal and lethal cancer owing to metastatic and relapsing disease. Currently, the role of microRNAs has been checked in tumorigeneses. Numerous studies have revealed that between the tumor suppressor miRNAs, the reduced expression of miR-146a-5p and -193a-5p in several cancers including CRC tissues are related with tumor progression and poor prognosis of patients. The purpose of this study is to examine the role of miR-146 a-5p and -193 a-5p in CRC cell cycle progression.

The miR-193a-5p and -146 a-5p mimics were transfected into HT-29 CRC cells via jetPEI transfection reagent and their impact was assessed on p53, cyclin B, and NF-kB gene expression. The inhibitory effect of these miRNAs on cell cycle was assessed by flow cytometry. The consequence of miR-193a-5p and miR-146 a-5p on the protein expression level of Murine double minute 2 (MDM2) was assessed by western blotting.

miR193a-5p and -146a-5p regulated the expression of MDM2 protein and p53, cyclin B, and NF-kB gene expression in CRC cells. Treatment of HT-29 cells with miRNA-146a-5p and -193a-5p induced G1 cell cycle arrest.

The findings of our study suggest that miR146a-5p and -193a-5p may act as a potential tumor suppressor by their influence on cell cycle progression in CRC cells. Thus, miRNA-146a-5p and -193a-5p restoration may be recommended as a potential therapeutic goal in the treatment of CRC patients.

The cytotoxic properties upon treatment with nicotine have been reported in several studies, but the underlying mechanisms remain not fully defined. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is one of the important nicotinic receptors, which nicotine partly by binding to this receptor exerts its effects. The current study aimed to investigates the influences of nicotine on cellular proliferative and apoptotic activities and tried to determine the involvement of α7nAChR in these functions.

Human hepatocellular carcinoma (HepG2) cell line was used to determine the individual or combined effects of treatments with nicotine (10 μM) and specific siRNA (100 nM) targeting α7nAChR expression. The MTT assay, DAPI staining assay, and flow cytometry assay were applied to measure the cell viability, apoptosis and cell cycle progression of the cells, respectively. In addition, the changes in the mRNA level of the genes were assessed by qRT-PCR.

Compared to control groups, the cells treated with nicotine exhibited significant dosedependent decreases in cell viability (log IC50 = -5.12 ± 0.15). Furthermore, nicotine induced apoptosis and cell cycle arrest especially at G2/M Phase. The qRT-PCR revealed that nicotine increased the mRNA levels of α7nAChR as well as caspase-3 and suppressed the expression of cyclin B1. Treatment with α7-siRNA abolished these effects of nicotine.

These experiments determined that upregulation of α7nAChR by nicotine inhibits HepG2 cells proliferation and induces their apoptosis. These effects blocked by treatment with α7-siRNA, which indicates the involvement of α7nAChR pathways in these processes.

Colorectal cancer (CRC) is attributed as one of the most common malignancies worldwide. CD133 molecule, as a pentaspan transmembrane glycoprotein, confers stem cell-related characteristics, including self-renewal and multi-directional differentiation capability. CD133 plays important roles in the progression of CRC by conferring apoptotic resistance and migration ability.

To investigate the antiapoptotic and anti-angiogenic effect of CD-133 targeted siRNA in a colorectal cancer cell line.

In this study, CD133-targeted siRNA transfection was conducted into HT-29 cells. MTT assay was employed to evaluate the cytotoxic effects of transfection on the cells. Flow cytometry was used to evaluate the apoptosis rate. The mRNA expression of apoptosis and metastasis related genes were assessed by quantitative Real-Time PCR (qRT-PCR). Wound healing assay was used to assess the migration potency of the infected cells.

Expression of CD133 was significantly downregulated after transfection of CD133-specific siRNA. Moreover, the rate of apoptosis was significantly increased after transfection. The migration potential of cells was diminished after transfection. siRNA delivery resulted in the modulation of expression of apoptosis and metastasis-related genes.

siRNA mediated targeting of CD133 could be considered as a promising approach to treat CRC through suppressing the cancerous behavior of tumor cells.

Lipid peroxidation is a prominent manifestation of free radical activity in biological systems, and it is involved in the development of different diseases such as cancer or cardiovascular and liver diseases. Malondialdehyde (MDA) is globally recognized as a scientifically accepted biomarker of oxidative stress. Due to the significance of MDA as a marker of lipid peroxidation and because of its elevations in various diseases, the assessment of MDA with new and reliable assays, the development of a fast, sensitive, and selective method to detect MDA with simple instruments is necessary. This study used the electro polymerization of a low toxic and biocompatible polymer with entitle poly arginine-graphene quantum dots-chitosan (PARG-GQDs-CS) as a novel strategy for surface modification of glassy carbon (GC) surface and preparation a new interface for measurement of MDA in human exhaled breath condensate (EBC). Nanocomposite PARG/CS/GQDs the method of precipitation out of place (ex situ) on the electrode surface was prepared. To verify sequestration nanobiopolymer synthesized Scanning electron microscope images (SEM) were recorded. To identify and study the behavior of malondialdehyde electrochemical methods such as cyclic voltammetry and differential pulse voltammetry were used. The scanning electron microscopy (SEM) images indicated immobilization of uniformly CS and GQDs onto PARG film. The modified electrode appeared as an effective electro activity for detection of MDA. Under the optimized analysis conditions and physiological pH, the prepared sensor showed one oxidation processes for MDA at potentials about 1 V vs. Ag/AgCl with a low limit of quantification (LLOQ) 5.94 nM. The Glassy carbon electrod modified by poly-arginine/chitosan/graphene quantum dots, has good electrical activity for Electro-oxidation malondialdehyde that could be due to synergistic effect poly-arginine, graphene quantum dots and chitosan to create many active sites for this purpose.

Cancer is a hyperactive disorder which can cause uncontrolled propagation of the cells. Several reports indicated that omega polyunsaturated fatty acids can prove their own antitumor effects on different cancerous cells by stopping the operation of the cellular cycle. Therefore, this study mainly aimed to investigate the impact of omega polyunsaturated fatty acids (PUFAs) on the exposition rate of genes CDK1, CyclinB1, and the cellular cycle of the stomach cancerous tissue in under-chemotherapy patients with stomach adenocarcinoma. The present study was a double-blind clinical trial in which neither the oncologist nor the patients were aware of the treatment before and after the intervention. The patients with stomach adenocarcinoma were first recognized and subjected to chemotherapy. A total of 24 patients were randomly selected and included in the case and control groups. The patients in the control group were treated with cisplatin and placebo while those of the case group first received cisplatin with the complementary capsule of fatty acids, namely, Natural Factors Ultimate Omega Factors with a dose of 1200 mg and 3600 mg daily, encompassing three 1200 mg medicines each course for 3 weeks. Three samples of the stomach biopsy were taken from all patients before and after the chemotherapy. All mRNA tissues were extracted out of the biopsy samples. Then, DNA was synthesized based on these samples and the exposition rate of the desired genes was measured using the real-time polymerase chain reaction (PCR) method. There was a significant decrease in the mean of exposition of the genes in the case group (P = 0.021) compared to the control group (P = 0.001). Generally, the results revealed that using omega fatty acids 3, 6, and 9 along with cisplatin medicine can be effective in stopping the cell cycle phase G2 in cancerous cells of the stomach tissue.

Gastric cancer is the 5th most common cancer and the third cause of death in the world. Studies have shown that gastric cancer is somewhat susceptible to chemotherapy, but the duration of tumour reduction is short, and patients have not had much success in survival, and in many cases, chemotherapy resistance has been observed. Therefore, the main objective of this study was to investigate the effect of omega-unsaturated fatty acids on the expression of Cyclin A2, and CDK2 germ cell cycle in patients with gastric adenocarcinoma under chemotherapy.

This is a double-blind, pre-and post-test clinical trial with the target population of patients with gastric adenocarcinoma that were first identified and subjected to chemotherapy. Twenty-four patients were selected randomly and randomly in control and control groups. In the control group, the treatment was routine with cisplatin plus placebo. In the case group, treatment with cisplatin plus a supplement of natural fatty acid supplementation capsules of Ultimate-Omega Factors with a dose of 1200 mg per day was 3,600 mg Three tablets of 1200 mg (for three courses) started on horizons three weeks. Three samples of stomach biopsy were taken from all patients before and after chemotherapy. Biopsy specimens were extracted from all tissue mRNAs and cDNA was synthesized from them, and then the expression of the genes was measured using Real-Time PCR. The results were analyzed by SPSS software version 24.

The mean or average expression of Cyclin A2, CDK2 in the case group showed a significant decrease compared to the control group (P value was 0.021 and 0.026, respectively.

The results of this study showed that the use of omega-3, 6, 9 fatty acids with cisplatin can be useful in stopping the S-cell cycle in gastric cancer cells.

CD20 is an important cell surface receptor that is used for target therapy of B cell lymphoma and some related blood diseases due to vital function of CD20. In previous studies, a Rituximab based humanized single chain variable fragment (scFv) antibody showed good reactivity against B cell related cancer cells. But this recombinant protein produced Inclusion Bodies (IBs) in Escherichia coli (E. coli) cytoplasm. The aim of this study was to investigate the effect of coexpression with cytoplasmic chaperones on expression and solubility of humanized anti-CD20 scFv in E. coli.
For this purpose, the fragment coding for anti-CD20 huscFv subcloned into the pET22b () and transformed into the E. coli BL21 (DE3) was evaluated. In order to inhibit the production of IBs, the effects of co-expression with cytoplasmic chaperones GroEL, DnaK, GroES, Tig, DnaJ and GrpE were investigated.
Coexpression with cytoplasmic chaperones led to increased soluble expression of anti-CD20 recombinant protein. Among investigated chaperones, pKJE7 chaperone plasmid containing DnaJ, GrpE, DnaK chaperone genes had significant effects with an expression yield of 325 µg/ml soluble anti-CD20 scFv.
The result of this study demonstrated remarkable effect of pKJE7 chaperone on enhancement of soluble expression of anti-CD20 huscFv antibody in E. coli.

T-cell acute lymphoblastic leukemia (T-ALL) is one of the most common malignancies associated with T-lymphocytes, accounting for 10 to 15 percent of ALL cases in children and 25 percent in adults. Innovative therapeutic approaches that overcome ineffective treatments on tumor cells may be a potential source of improvement in therapeutic approaches. Suppression of gene expression at transfusion level is one of the important strategies in gene therapy. The expression of PTPN22 and miR-181 genes in all types of hematologic malignancies increases and is likely to contribute to the survival and death of cells by affecting a variety of signaling pathways. The purpose of this study was to determine the role of PTPN22 inhibition by siRNA, and alteration in miR-181a and miR-181b in Jurkat cell line.
Jurkat cells were transfected with 80 pmol of siRNA to inhibit PTPN22. After that, expression of PTPN22 mRNA and transcript levels of miR-181a and miR-181b were measured with Real-time PCR after 48hrs.
Experiments demonstrated that siRNA transfection resulted in significant downregulation of PTPN22 mRNA after 48 hrs in 80 pmol dose of siRNA. Moreover, transcript levels of both miR-181a and miR-181b was decreased after transfection.
PTPN22, miR-181a and miR-181b might be involved in progression of Jurkat cells and targeting these molecules by RNAi might confer promising tool in treatment of T-ALL.

Surface layer as the outer protective coverage of bacteria and archaea are two-dimensional crystalline and symmetrical arrays of proteins that recently attract a lot of attention for biologist scientists. The surface layers of bacteria are usually 5 to 10 nm in diameter and represent highly porous protein lattices with uniform size and morphology with the pore sizes of 2 to 8 nm. The crucial and most prominent property of this protein-based layer is the regular morphology and suitable chemical composition for different biological applications. Although the formation mechanism of surface layers is different from one type of cell to another once, the surface layer protein molecular compositions almost are same for all types. Recently, the biological application of surface layers opens a prominent research fields in surface biological science such as nano-biotechnology adhesion, vaccination, pharmaceutical, biosensors, bioremediation and mineralization application. In this mini review, we discussed about the main application of this nano-layer in biological systems.

The use of mesoporous nanomaterials as hosts for polymers production is a field of great interest, especially in the case of conducting polymers. Free-radical polymerization inside mesoporous silica has been investigated in order to open a route to functional polymer-silica composite materials with well-defined mesoporosity. In this report, proline monomers integrated with beta cyclodextrin were electropolymerized into amino functionalized mesoporous silica. The fabrication of poly-proline-amino functionalized magnetic mesoporous silica-beta cyclodextrin nanohybridon glassy carbon electrode was performed using one step electrodeposition regime. Field emission scanning electron microscopy was confirmed produced nano-hybrid material containing poly-proline into the pores of amino functionalized mesoporous silica which leads to increase of surface coverage of poly-proline. The results indicate that Poly-proline was successfully generated inside the pores of the amino functionalized MCM-41 and that the amine group was capable of protonating the polymer, producing poly-proline, the most conductive one, without the addition of another acid source during the polymerization step. The grafted amine groups also promoted a stronger interaction between inorganic matrix and proline than the observed in nano-encapsulated poly-proline, which resulted in high conductively. Therefore, it was evaluated some electrochemical aspects of the prepared nano-hybrid using cyclic voltammetry, differential pulse voltammetry and linear sweep voltammetry. Finally, the electroactivity of poly-proline-amino functionalized magnetic mesoporous silica-beta cyclodextrin nano-hybrid modified glassy carbon electrode towards detection and determination of some physiologically-relevant electroactive small molecules, was studied. Furthermore, it is demonstrated that the nano-coatings of polymers deposited on the mesopore walls have remarkably enhanced sensitivity and selectivity, as compared to that of bulk polymer resins. We believe that, due to facile functionalization and attractive textural properties, the mesoporous polymer-silica composite materials are very useful for biomedical applications.

As a laboratory technique, the analysis of amino acid plays an important role in biochemical, pharmaceutical and biomedical fields. There is, therefore, a need for the rapid and accurate analysis of amino acid. In this report, the Fe3O4 magnetic nanoparticles/graphene quantum dots (Fe3O4 MNP-GQDs) was used for the investigation of electroactive amino acids effect on the electrochemical signals of each other. This sensor used towards probing the interaction study of electroactive amino acids with each other at physiological pH (pH=7.4) by differential pulse voltammetry. The herein described approach is expected to promote the exploitation of electrochemically-based methods for the study of amino acids-amino acid interaction which is necessary in biochemical and biosensing studies. This report may open a new window to direct peptide analysis in the future.

Nearly all of flavonoids are good metal chelators and can chelate many metal ions to form different complexes. This article describes a synthesis of Quercetin–Tb(III) in methanol, characterized by using elemental analysis, UV–visible and evaluation of its antioxidant properties. The formation of complexes is realized from the UV–visible spectra which shows that the successive formation of Quercetin–Tb(III) occurs. To find out the antioxidant activity variation and the role of Tb(III) ion on the antioxidant activity of the complexes different radical scavenging methods such as: 1,1-diphenyl-2-picrylhydrazyl (DPPH), ferric reducing antioxidant power (FRAP) and 2,2′-azinobis 3-ethylbenzothiazoline-6-sulphonic acid (ABTS) were used. The results from DPPH, ABTS and FRAP methods showed that Quercetin and Quercetin–Tb(III) complex are capable of donating electron or hydrogen atom, and consequently could react with free radicals or terminate chain reactions in a time- and dose-dependent manner. This study showed that the chelation of metal ions by Quercetin decrease the redox potential of Quercetin-metal complex.